Motion sickness, spatial disorientation and vertigo have been acknowledged as a wide-spread problem, affecting a significant portion of world population to varying degrees. Researchers report that up to 60% of the population have some motion intolerance. It has been reported that motion sickness affects nearly one third of all people who travel by land, sea, or air. Individuals are affected daily by motion sickness and spatial disorientation while riding in automobiles, trains, buses, planes or other transport. The Greeks provided the first written historical account of motion sickness. The Roman Cicero claimed he would rather be killed in battle than suffer the tortures of nausea maxis. Motion sickness has even been used as a form of punishment. One of the world's most famous mariners, Admiral Lord Nelson reportedly never adapted to motion sickness. Napolean's General Carbuccia refused to use camels for Napoleon's army, because of the issues with motion (2) Even Lawrence of Arabia is reported to have experienced Camel sickness.
It is also known that some people are more susceptible than others; for example, women are more sensitive to motion than men by a ratio of about 5:3. Some are more susceptible due to physical reasons such as age. Studies show a significant genetic contribution to a propensity to motion sickness. It has been well observed that poor ventilation, bad odors, smoking, eating large fatty meals and alcohol can make motion sickness more pronounced. Susceptibility to motion sickness begins at about age two, and for most will peak in adolescence and decline gradually. However, many adults remain highly sensitive caused by any motion, particularly when combined with either an absence of a visual reference or to significant levels of visual stimuli. In fact, a provocative visual stimulus has been shown to be the most influential cause of motion sickness symptoms. Reading in a moving vehicle, abruptly moving the head (such as looking down) while a vehicle is moving can provoke symptoms. Fear, anxiety and other psychological factors can contribute to the onset of motion sickness. Some people can get sick just thinking about an upcoming trip or flight.
For those who experience the symptoms, the result is often disabling, with nausea, vomiting, sweating, and unsteadiness, while feeling cold, clammy and disorientated. In addition, the term “sopite syndrome” was coined to refer to the apathy, passivity, and lack of concentration characteristic of motion sickness.
The occurrence of motion sickness can approach 100% in cruise ship passengers on rough seas. Seasickness, a common form of motion sickness, is frequent among naval personnel, where 60% to 90% percent of inexperienced sailors can suffer from seasickness. Experienced crew-members are not immune. Up to 60% of experienced crew-members have been affected in these conditions. This becomes a major problem in modern seamanship in which small crews are responsible for the operation of sensitive and sophisticated equipment. During the invasion of Normandy, in World War II, the seas were reportedly very high causing the landing crafts to pitch and yaw, like a kite in a windstorm. The soldiers were lying and sitting in flat bottomed crafts and were using huge buckets for vomiting and urinating, which soon overflowed after boarding. As thousands of men were lying in the vomit, urine and rain they debarked in a state of terror, which was compounded by their symptoms of seasickness, and attempted to perform at a high level in order to survive in combat. Many of these soldiers had to overcome the most debilitating effects of motion sickness to survive. Volumes of data documents motion sickness's severe effect on human performance of even basic tasks.
Spatial disorientation along with motion sickness are significant problems in aviation. In motion provocative environments, spatial disorientation and motion sickness cause not only a loss in human performance (affecting cognitive and motor skills), but a loss of expensive aircraft and human life. Thousands of deaths have been attributed to aviation accidents caused by being spatially disoriented. A recent study has shown that almost Ninety to One Hundred percent (90-100%) of aircrew have reported at least one incidence of spatial disorientation (SD) during their flying careers. SD accounted for Eleven to Fourteen percent (11-14%) of USAF mishaps and a mishap fatality rate of 69%, with risk of SD significantly increased in helicopters and fighter/attack aircraft and at night. The most frequent experienced SD episodes are “leans” (Ninety-Two percent (92%)), loss of horizon due to atmospheric conditions (Eighty-Two percent (82%)), misleading altitude cues (Seventy-Nine percent 79%)), sloping horizon (Seventy-Five percent (75%)), and SD arising from distraction (Sixty-Six percent (66%)). In a review of aviation mishaps from 1987-1997 there was an average of one fatal SD accident every Eleven (11) days in the United States. The death of John F. Kennedy Jr. was an example of a spatial disorientation accident and unknown to many were thirty other reported crashes that same day, with at least one other due to spatial disorientation. According to FAA statistics, SD and loss of situational awareness causes Fifteen to Seventeen percent (15%-17%) of fatal general aviation crashes annually. More significantly, Nine (9) out of ten (10) SD mishaps result in a fatality. The Air Force Safety Center FY93-02 mishap analysis reported that Class A mishaps resulted in Two Hundred Forty-Three (243) destroyed aircraft, Three Hundred Ten (310) fatalities, and an economic loss of Six Billion Two Hundred Thirty Million dollars ($6.23 billion). Airsickness has also been identified as a flight training issue. A motion sickness history questionnaire obtained from student pilots in the Air Force revealed an incidence of airsickness of fifty percent (50%). In a questionnaire to B-1 and B-52 bomber crewmembers, it was reported to be a frequent occurrence among non-pilots in both aircraft, and experienced crewmembers were more likely to report an impact on their duties.
Space motion sickness is experienced by Sixty to Eighty percent (60%-80%) of astronauts during the first Two to Three (2-3) days in microgravity and by a similar proportion during their first few days after return to Earth. Up to Ninety percent (90%) of astronauts experience spatial disorientation during reentry and landing of the shuttle, with prevalence proportional to the length of the mission. Exposure to microgravity rearranges the relationships among signals from visual, skin, joint, muscle, and vestibular receptors. Congruence between vestibular signals and those from other receptors, as well as between the vestibular otolith and semicircular canal receptors, is disrupted by the absence of gravity. This lack of congruence between sensory exposure to provocative real or apparent motion leads to the progressive cardinal symptoms of terrestrial motion sickness. Space motion sickness may vary slightly with flushing more common than pallor, stomach awareness, malaise, loss of appetite, and sudden vomiting, often without prodromal nausea.
Simulator sickness is another example of motion sickness, and many military pilots have reported at least one symptom following simulator exposure. In a study of Coast Guard aviators undergoing flight simulator testing, Sixty-Four percent (64%) reported adverse symptoms during the first simulator flight and Thirty-Nine percent (39%) did so during the last flight. Thirty-Six percent (36%) of pilots reported motion sickness when training on a Blackhawk flight simulator.
More recently, simulator sickness in virtual environments (VE) has become an important issue. Virtual reality is already a popular technology for entertainment purposes, and both the U.S. Army and Navy are interested in the training applications of virtual environments. However, some users of VE experience discomfort during, and sometimes after, a session in a simulated environment, in equivalent fashion to simulator sickness already noted for flight and driving simulators.
There have been many theories about the cause of motion sickness, spatial disorientation and vertigo. The earlier Gut Theory proposed that vomiting was a reflex response to irritation of the gastric mucosa possibly caused by movements of the viscera which caused abdominal contractions and over-stimulated the Pacinian corpuscles or overproduction of bile in the liver. There are also Vascular or Blood Theories: those that proposed a lack of blood flow to the brain (cerebral anemia) and those that proposed too much blood going to the brain (cerebral hyperemia). These conditions were theorized to be caused by numerous mechanisms. One such theory suggested that vascular deficiency was due to the irritation of the eyes by perceived motion, which, by reflex action, produced spasm in the cerebral capillaries causing giddiness and vomiting. Other vascular theories argued that motion produced cerebral hyperemia, which destabilized brain cells in the vomiting center of the medulla oblongata.
Other theories attributed it to respiratory factors, shock to the central and autonomic nervous system, or due to infections. The vestibular and other sensory contributions came later, and were built upon some of the early work of Purkinje, Flourens, and Meniere.
Over-stimulation of the semicircular canals theory evolved in the 1990s. This lost favor when it became clear that motion in the absence of vestibular stimulation could be as provocative as the primary sensory organs.
A fluid shift theory with assumptions of active or passive shifts in the body fluids to the central nervous system and vestibulo-auditory mechanisms was considered a cause in space flight.
The neural mismatch theory suggested the problems to be in the central integrative mechanism, which is involved in interpreting the significance of the sensory environment. It was proposed that the conflict between visual or vestibular input systems or between separate components of the vestibular system is of secondary importance to mismatch occurring between ongoing sensory experience and long-term memory. The limbic system was suspected as perhaps being the neural mismatch center of the brain.
Currently, the sensory conflict theory appears to be the dominant theory favored by researchers in that the majority of investigators agree that it is not solely the movement or movement stimulus that results in motion sickness, but rather a conflict in movement information detected by the different sensory modalities of the inner ear, vision, and proprioception. A conflict of visual and vestibular (inner ear) information, as it relates to postural control and visual stabilization, is certainly a critical factor. Investigators now also agree that it is primarily an incongruence of visual and vestibular sensory information regarding movement and orientation that results in motion sickness. Incongruence between the semicircular canals and the otolithic organ input has also been implicated as the provocative stimulus in seasickness and in the onset of motion sickness associated with weightlessness. Another contributing factor which may trigger susceptibility to motion sickness may be the mass size differences of the utricular otoconia between the left and right sides in some people, as seen in fish.
Within the sensory conflict concept has arisen an ‘incongruence in the visual system’ theory which can be called a Velocity Storage Theory. The vestibular nerve communicates head velocity and estimates of angular displacements require further central nervous system processing (i.e. integration). There is some inconsistency between velocity-based ocular studies and displacement-based perceptual studies. Most oculographic studies of vestibular function are based on measurements of the slow phase velocity of the eye. If a monkey or man is rotated at constant velocity in the dark, the velocity of the slow phase of the nystagmus decays exponentially with a time constant of Fifteen to Twenty seconds (15-20 sec). Direct recordings of the vestibular nerve in monkeys have shown the head velocity signal, transmitted by the vestibular nerve, has a time constant of decay of only Seven to Ten (7-10 sec). The duration of the eye velocity curve (i.e. a nystagmus response) is therefore longer, outlasting the sensation or perception curve. The perception of angular velocity is based on signals subserved by the brainstem velocity storage system. Thus the head velocity signal appears to be stored in the brain and then released onto ocular motor neurons for the generation of nystagmus. Brainstem circuits in the vicinity of the vestibular nuclei, behaving as mathematical integrators, are thought to mediate this storage process. There is evidence that motion sickness is generated through this velocity storage and can be reduced by reducing the angular vestibular ocular reflex time constant. Others support a multi-factor explanation of motion sickness, involving both sensory conflict and eye movement.
Vestibular Dysfunction. Postural control requires a complex interaction of visual and proprioceptive sensory inputs providing external orientation reference frames while the internal reference frame is provided by the vestibular system. An estimated Twenty percent (20%) of the general population is affected by a vestibular disorder. Ninety million (9 million) Americans (Forty-Two percent (42%) of the population) will complain of dizziness at least once during lifetime, and, of these, Eight percent (80%) will have a vestibular component. There are more than Ten million (10 million) physician visits annually for dizziness or balance complaints (National Balance Centers/Vestibular Disorders Association), with a cost of greater than one billion dollars per year. Persistent vestibular dysfunction can occur following a variety of insults to the vestibular system, including infections, ototoxicity, trauma, chronic ear pathology, tumors, Meniere's disease, surgery and other idiopathic causes. Acoustic tumor surgery and vestibular nerve section, performed for disabling vertigo in patients with Meniere's disease, usually result in rapid compensation. However some patients, particularly non-Meniere's disease patients, have a prolonged period of unsteadiness without compensation for a long period of time. The resulting disability can be devastating. It has also been shown that postural instability precedes motion sickness with provocative visual stimuli. All these vestibular impairments cause disequilibrium, blurred vision, disorientation, and vertigo, which in turn cause dysfunction in many activities of daily living and in social interactions that traditional medical treatments may not address.
Mismatches can be caused where there is a mismatch between stimuli as processed by the brain. Mismatches can occur where there is motion, or where there is no motion. These mismatches may be caused by delays in the delivery or processing of the stimuli or mismatch of stimuli even without delay. Examples of mismatches are seen in persons suffering from vertigo or persons in a virtual space such as a video game or flight simulator or targeting system.
Butnaru in U.S. Pat. No. 5,966,680 taught the use of a device and method which operates as an artificial labyrinth to eliminate sensory mismatch between a person's natural labyrinth vestibular system and the vision system of the user. The device provided the user with an alternative means for determining true orientation within his environment through a system of visual cues. However Butnaru system of cues have been determined to have some limitations and the Butnaru system is lacking in its integration with user environments, which may cause sensory mismatches.
There is a need for improvements to systems which avoid vertigo, motion sickness, and spatial disorientation integrated in motion sensory provocative environments to avoid problems associated with compromised human performance or even loss of user control.